描述：
TL1A is a type II transmembrane protein belonging to the TNF superfamily and has been
designated TNF superfamily member 15 (TNFSF15). Human TL1A is a 251 aa protein
consisting of a 35 aa cytoplasmic domain, a 24 aa transmembrane region and a 192 aa
Cterminal extracellular domain. It is a longer variant of the previously cloned TL1 (also
known as VEGI) that is possibly a cloning artifact. TL1A is predominantly expressed in
endothelial cells and its expression is inducible by TNF-α and IL-1α. TL1A binds with high
affinity to death receptor 3 (DR3), which is now designated TNF receptor superfamily member
25 (TNFRSF25). DR3 was formerly designated TNFRSF12 when it was thought to be the receptor
for TWEAK/TNFSF12. DR3 is expressed primarily on activated T cells. Depending on the cell
context, ligation of DR3 by TL1A can trigger one of two signaling pathways, activation of the
transcription factor NF-kappa-B or activation of caspases and apoptosis.On primary T cells,
TL1A induces NFkappaB activation and a costimulatory signal to increase IL-2 responsiveness
and the secretion of proinflammatory cytokines. However, in a tumor cell line, TF-1, TL1A has
been shown to induce caspase activity and apoptosis. These effects of TL1A are blocked by the
secreted, soluble decoy receptor 3 (DcR3), also known as TR6 and TNFRSF6B, which compete
with DR3 for binding to TL1A. Consistent with the observed in vitro activities, TL1A promotes
ex vivo splenocyte expansion and enhances in vivo graft-versus-host-response.
原厂资料：
TL1A is a type II transmembrane protein belonging to the TNF superfamily and has been
designated TNF superfamily member 15 (TNFSF15). Human TL1A is a 251 aa protein
consisting of a 35 aa cytoplasmic domain, a 24 aa transmembrane region and a 192 aa
Cterminal extracellular domain. It is a longer variant of the previously cloned TL1 (also
known as VEGI) that is possibly a cloning artifact. TL1A is predominantly expressed in
endothelial cells and its expression is inducible by TNF-α and IL-1α. TL1A binds with high
affinity to death receptor 3 (DR3), which is now designated TNF receptor superfamily member
25 (TNFRSF25). DR3 was formerly designated TNFRSF12 when it was thought to be the receptor
for TWEAK/TNFSF12. DR3 is expressed primarily on activated T cells. Depending on the cell
context, ligation of DR3 by TL1A can trigger one of two signaling pathways, activation of the
transcription factor NF-kappa-B or activation of caspases and apoptosis.On primary T cells,
TL1A induces NFkappaB activation and a costimulatory signal to increase IL-2 responsiveness
and the secretion of proinflammatory cytokines. However, in a tumor cell line, TF-1, TL1A has
been shown to induce caspase activity and apoptosis. These effects of TL1A are blocked by the
secreted, soluble decoy receptor 3 (DcR3), also known as TR6 and TNFRSF6B, which compete
with DR3 for binding to TL1A. Consistent with the observed in vitro activities, TL1A promotes
ex vivo splenocyte expansion and enhances in vivo graft-versus-host-response.
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